Amplification of the MT1gene in some breast tumors and an inverse correlation with ERalpha, PR and MT1 G protein-coupled melatonin receptor.

NQO2 is a newly discovered binding site (MT3) of melatonin, indicating that it could be a novel target for prevention of breast cancer initiation.

N(4-chlorobenzoyl)melatonin as a specific AKR1C3 inhibitor validate its role in the proliferation of breast cancer cells.

Shift-work has been associated with breast cancer, due to a circadian disruption and to a nocturnal suppression in melatonin production.

In breast cancer risk, melatonin may also block the estrogen receptor ERalpha and impact the enzyme aromatase, which produces estradiol.

Melatonin inhibits the growth of breast cancer by interacting with estrogen-signaling(SERM)-(SEEM) pathways.

Studies suggest that a shortened duration of nocturnal sleep,circadian phase shifts, nocturnal melatonin suppression are associated with a higher risk of breast cancer development.

Use of MDB as the first line therapy, in a patient which had not been debilitated by the effects of chemo-and radiotherapy, contributed greatly to the final outcome.

An increased concentration of urinary aMT6s was associated with a lower risk of breast cancer.

Two distinct apoptotic processes are triggered by melatonin(1 nM), an early, TGFbeta1 and caspase-independent response, and a late TGFbeta1-dependent process in which activated-caspase-7.